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BMS 242 - Phys and pharm of cells > Advanced muscle physiology > Flashcards

Advanced muscle physiology Flashcards

1
Q

What is a muscle fascicle?

A

Bundle of skeletal muscle fibres, which are subdivided into myofibrils

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2
Q

What are myofibrils spilt into?

A

Sarcomeres that are made are myofilaments

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3
Q

What forms the Z-line in muscle?

A

Alpha activin

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4
Q

What are the 2 key proteins between the z lines?

A

Actin (thin)

Myosin (thick)

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5
Q

What does the muscle contraction dependant on?

A

The overlap between the actin and the myosin

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6
Q

What is the ‘cross bridge theory’?

A

‘The tension in a muscle is dependant on the area of overlap between the actin and myosin’

The greater the overlap –> the greater cross-bridges can form –> the greater the degree of contraction

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7
Q

What happens to the Z bands as the muscle contracts?

A

They become CLOSER together

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8
Q

What does the neuronal potential cause in the muscle when it arrives?

A
  • Generation of an action potential in the muscle
  • Leads to the activation of voltage gated Ca2+ channel –> increase in intra cellular Ca2+
  • Ca2+ is critical in the sliding myofilament hypothesis –> causes contraction
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9
Q

What is the site of the neuronal action potential –> muscle action potential?

A

In the NEUROMUSCULAR JUNCTION

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10
Q

What is the neuromuscular junction?

A

A muscle cell and an un-myelinated neuron

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11
Q

What is a motor unit?

A

ONE motor neuron and the muscle FIBRES its innervate

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12
Q

What is the difference between fine control and gross control of muscle contraction

A

Fine - one motor neuron innervate a small number of fibres

Gross - one motor neuron innervate a large number of fibres

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13
Q

How many motor units are in an individual muscle?

Why is this advantageous?

A

MANY motor units

The more motor units a muscle has –> the more fine control –> the bigger range in the degree of muscle

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14
Q

What neurotransmitter is critical for the normal function of the NMJ?

A

Ach

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15
Q

What ion channels are involved in the action potential in the NMJ?

What do these channels mediate?

A

Nav - mediate depolarisation of the AP

Kv - mediates the repolarisation of the AP

Cav - mediates the increase in intracellular Ca2+ which drives the FUSION of the vesicles containing Ach to the presynaptic membrane

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16
Q

What are the Cav channels activated by?

A

Depolarisation of the neuron

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17
Q

What does Ach released into the synaptic cleft (from the motor neuron) do?

What does this cause?

A

Bind to NICOTINIC Ach receptors on the post synaptic membrane (muscle fibre)

  • Causing depolarisation of the muscle fibre membrane and the activation of Nav
  • Activates Cav
  • Leads to the influx of Ca2+ into the muscle fibre
  • -> muscle contraction
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18
Q

What is the length of a skeletal action potential?

What is this the same as?

A

1-2ms

Same as the neuronal action potential

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19
Q

Describe the action potential in the skeletal muscle

A
  • Activation of Nav –> increase in permeability of the membrane to Na+
  • -> Drives the membrane potential to Ena (+60mV)
  • Muscle fibre to threshold –> activates Kv channels
  • -> Drives the membrane potential to Ek (-90mV)
  • Re polarisation of the membrane due the closure of Nav channels and the opening of Kv channels
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20
Q

What conductance measured in?

A

Mili Siemens/cm^2

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21
Q

What increases the conductance of a channel?

A

The more ions that move through the channel

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22
Q

What does depolarisation activate?

A

1) Opening of the Nav channels
2) Closure of the Nav channels (slower)
3) Inactivation of the Nav channels (slower)
4) Activation of the Kv channels (slower)

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23
Q

What are the 2 forms of the AchR?

A

1) Nicotinic

2) Muscarinic (GPCR)

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24
Q

What is the nicotinic AchR?

A

A non-selective CATION CHANNEL

Permeable for: Na+, Ca2+, K+

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25
Q

What is the Nerst potential for the nicotinic AchR?

A

~0mV

26
Q

What happens when the nicotinc AchR channel is open?

A

Drives the membrane potential to 0

27
Q

Is activation of the nicotinic AchR alone enough to cause an action potential?

A

NO - it is only a trigger for Nav, which causes the depolarisation of the membrane

28
Q

What is the structure of the nicotinic AchR?

A
  • 4 different types of subunit
  • 5 subunits need to come together to make a functional channel (pentameric)
  • Each subunit has 4 transmembrane spanning domains
  • N and C are EXTRACELLULAR
  • 2 binding sites for Ach
29
Q

What subunits must come together to make a functional channel?

A

MUST have 2 x alpha subunits

With a variety of other subunits

30
Q

Why can there be many different types of nicotinic AchR?

A

Variety of subunits can come together with 2 x alpha subunits to make MANY different channels with different structures

31
Q

How many genes code for different alpha subunits?

What are they?

A

9 different genes (9 different subunits)

CHRNA1 - CHRNA9

32
Q

Which alpha subunit(s) are found in the skeletal muscle?

A

CHRNA1

33
Q

Which alpha subunit(s) are found in the neuronal tissue?

A

CHRNA2 - CHRNA8

34
Q

How many genes code for different beta subunits?

What are they?

A

4 different genes (4 different subunits)

CHRNA1 - CHRNA4

35
Q

Which beta subunit(s) are found in the skeletal muscle?

A

CHRNA1

36
Q

Which beta subunit(s) are found in the neuronal tissue?

A

CHRNA 2-4

37
Q

What do the properties of the AchR depend upon?

A

Depend upon the subunits that come together

38
Q

How many molecules of AchR are needed to bind to the nicotinic receptor in order for it to open?

A

2

39
Q

What is Myasthenia gravis?

A

AUTOIMMUNE dIsease of the NMJ

40
Q

What is the background behind Myasthenia gravis?

A
  • Antibodies target the A1B1 AchR on the postsynaptic membrane of the NMJ
  • Bind and block this receptor –> leading to DEGRADATION of the AchR
  • Less likely to get an action potential and muscle contraction
41
Q

What are the symptoms of Myasthenia gravis?

What can these symptoms lead to?

A
  • Skeletal muscle weakness and tiredness

- Can lead to RESPIRATORY FALIURE

42
Q

What are 6 treatments for Myasthenia gravis?

A

1) Acetycholinesterase inhibitors
2) Immunosupressants
3) Plasmapheresis
4) Corticosteroids
5) IV immunogloulins
6) Thymectomy

43
Q

When are acetycholinesterase inhibitors used to treat Myasthenia gravis?

How do they work?

A

MILD symptoms

  • INHIBIT AchE which breaks down Ach in the synaptic cleft
  • -> Ach stays around for as long as possible to maximise the activation of the nicotinic AchR
44
Q

What is an example of an AchE inhibitor?

A

Pyridostigmine

45
Q

How do immunosuppressants treat Myasthenia gravis?

Example?

A

Suppress the PRODUCTION of the antibodies against AchR

Cyclosphorin

46
Q

When is plasmapheris used to treat Myasthenia gravis?

How does it work?

Process?

A

When acute intervention is needed (symptoms are life-threatening)

Removes the antibodies from the plasma

Filtration of the blood using IMMUNOADSORPTION

  • Molecules on the filter bind the antibodies by mimicking the AchR
  • Reducing antibody levels
47
Q

What are corticosteroids used to treat Myasthenia gravis?

How does it work?

A

For moderate to serve symptoms

Immunosupressant

48
Q

What are the side effects of corticosterioids?

A

From suppressing the immune system

49
Q

When are IV immunoglobulins used to treat Myasthenia gravis?

How?

A

For SEVERE symptoms

  • Allows the immunoglobulins in the patients blood to ‘mop up’ the antibodies
  • Cannot bind to the AchR
50
Q

What is thymectomy?

Why is this done to treat Myasthenia gravis?

A

Removal of the thymus

Some patients have tumours here
Remove the thymus - removal of the AchR antibody secreting cells B-cells

51
Q

What happens when AchE inhbitors are injected into mice with antibodies against Ach?

A

Mice can stand up –> have better motor function

52
Q

What are T-tubules?

What are they important in?

A

Membrane invaginations in the skeletal/cardiac muscle

Important in:
- AP propagation into myofibrils

  • Taking the AP from the muscle fibre membrane to the sarcoplasmic reticulum (deep in the muscle where the Ca2+ is stored)
53
Q

What is a ‘triad’?

A

T-tubule with the sarcoplasmic reticulum either side

54
Q

What channels sit in the T-tubule membrane?

How do they sit?

A

L-type voltage gated Ca2+ channels

In an array of 4

55
Q

What happens to the L-type voltage gated Ca2+ channels as the T-tubule membrane depolarises?

What does this allow?

A

The L-type channels are activated

Causes:
1) Ca2+ FROM the extracellular fluid (contained within the T-tubules) into the cells

2) The opening of the Ryanodine receptors (another type of Ca2+ channel) in the SR

56
Q

How does the activation of the L-type Ca2+ channel cause the opening of the Ryanodine receptor channel?

A

These channels are coupled together:

  • As the L-type channels open –> mechanical process opens the Ryanodine receptors
57
Q

What happens when the Ryanodine receptors in the SR are opened?

A

Ca2+ from the SR store into the cytosol –> muscle contraction

58
Q

As well as via L-type Ca2+ channels, how else can Ryanodine receptors be activated?

A

Ca2+ induced release:

  • Ca2+ from OUTSIDE the cell activates the Ryanodine receptors
  • Leading to Ca2+ release from the store
59
Q

Why must Ca2+ be removed from the muscle following contraction?

A

To allow the muscle to relax and be able to contract again

60
Q

How is Ca2+ removed from the muscle?

A

1) Ca2+ ATPase
2) Na+/Ca2+ exchanger
3) Uptake of Ca2+ back int the SR
4) Ca2+ binding proteins in the SR

61
Q

What are the 3 different types of Ca2+ ATPase?

A

SERCA
PMCA
SPCA

62
Q

How does the Na+/Ca2+ exchanger lower intracellular Ca2+?

A

1 Ca2+ out for every 3 x Na+ in

BMS 242 - Phys and pharm of cells (13 decks)

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